SynthesisNature communications2018
Identification of multiple risk loci and regulatory mechanisms influencing susceptibility to multiple myeloma.
Synthesis in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. It is linked to trial NCT05539079 (A Prospective Long-term Observational Study in Patients With Monoclonal Gammopathy of Undetermined Significance), which is not on this map. Cited by 75 papers, 4 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
A Prospective Long-term Observational Study in Patients With Monoclonal Gammopathy of Undetermined Significance
Who cites it
75 citing papers in PubMed, 4 syntheses or guidelines pooled it, 113 citations in OpenAlex.
- Polymorphisms within Autophagy-Related Genes as Susceptibility Biomarkers for Multiple Myeloma: A Meta-Analysis of Three Large Cohorts and Functional Characterization.International journal of molecular sciences · 2023Pooled it
- Genome-wide meta-analysis of monoclonal gammopathy of undetermined significance (MGUS) identifies risk loci impacting IRF-6.Blood cancer journal · 2022Pooled it
- A meta-analysis of genome-wide association studies of multiple myeloma among men and women of African ancestry.Blood advances · 2020Pooled it
- Transcriptome-wide association study of multiple myeloma identifies candidate susceptibility genes.Human genomics · 2019Pooled it
- A prospective study of familial predisposition to plasma cell dyscrasias.Blood advances · 2026Article
- Genetic architecture of multiple myeloma: From somatic alterations to germline susceptibility and clinical implications.Translational oncology · 2026Review
- Article
- Profile of biological aging in first primary cancers: a pan-cancer analysis of two large-scale cohorts from the UK and Hong Kong.BMC medicine · 2025Article
- Clustering of lymphoid neoplasms by cell of origin, somatic mutation and drug usage profiles: a multi-trait genome-wide association study.Blood cancer journal · 2025Article
- Polygenic Risk, Agent Orange Exposure, and Lymphoid Neoplasms in the Veterans Affairs Million Veteran Program.JAMA network open · 2025Article
- Therapeutic Target Discovery for Multiple Myeloma: Identifying Druggable Genes via Mendelian Randomization.Biomedicines · 2025Article
- Addressing Health Disparities in Hematologic Malignancies: from Genes to Outreach.Blood cancer discovery · 2025Review
- FaMMily Affairs: Dissecting inherited contributions to multiple myeloma risk.Seminars in hematology · 2025Review
- Germline predisposition in multiple myeloma.iScience · 2025Article
- Expression quantitative trait loci influence DNA damage-induced apoptosis in cancer.BMC genomics · 2024Article
- Mosaic chromosomal alterations in hematopoietic cells and clinical outcomes in patients with multiple myeloma.Leukemia · 2024Article
- Sequence variants influencing the regulation of serum IgG subclass levels.Nature communications · 2024Article
- Deciphering the genetics and mechanisms of predisposition to multiple myeloma.Nature communications · 2024Article
- Multiple myeloma.Nature reviews. Disease primers · 2024Review
- Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
70 authors at 20 institutions in 19 countries.
Funding
Abstract
Genome-wide association studies (GWAS) have transformed our understanding of susceptibility to multiple myeloma (MM), but much of the heritability remains unexplained. We report a new GWAS, a meta-analysis with previous GWAS and a replication series, totalling 9974 MM cases and 247,556 controls of European ancestry. Collectively, these data provide evidence for six new MM risk loci, bringing the total number to 23. Integration of information from gene expression, epigenetic profiling and in situ Hi-C data for the 23 risk loci implicate disruption of developmental transcriptional regulators as a basis of MM susceptibility, compatible with altered B-cell differentiation as a key mechanism. Dysregulation of autophagy/apoptosis and cell cycle signalling feature as recurrently perturbed pathways. Our findings provide further insight into the biological basis of MM.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.